13. HYPERTENSIVE CRISIS Flashcards
Definiition
Hypertensive crisis is a sudden, acute blood pressure elevation levels higher than what is normal for the infected individual. BP > or equal 180/120
It is classified into two types:
1. Hypertensive urgency
2. Hypetensive emergency
Both of which can develop Patience with or without known pre-existing hypertension
HYPERTENSIVE URGENCY - severe BP elevation WITHOUT progressive target organ damage, hence the new term, SEVERE ASYMPTOMATIC HYPERTENSION
This is usually a consequence of non-adherence to anti-hypertensive medications as well as to low sodium diet and requires reduction of BP within a few to 24 hours with ORAL medications
On the other hand, HYPERTENSIVE EMERGENCY is a severe elevation In blood pressure less common complicated by evidence of impending or progressive target organ damage.
This requires immediate but gradual reduction in BP by approximately 10 to 20% in the first hour and additional 5 to 15% over the next 23 hours using IV medication.
major exceptions include:
1. Patient is the acute phase of ischemic stroke who are the candidates for reperfusion therapy but with BP of more than or equal to 185/100 or those who are NOT candidates but with BP > or = 200 mmHg/120
- Patience with intracerebral hemorrhage with SBP >200 mmhg or SBP >180 but with evidence of increased ICP, BP must be aggressively reduced without compromising tissue/cerebral perfusion pressure
- Patience with acute aortic dissection we’re in SVP must be lowered to a target of 100-200 mmhg within 20 minutes to reduce aortic shearing forces
Nevertheless, it Is important that the blood pressure be lowered only at a rate by which tissue perfusion can be maintained by AUTOREGULATION To prevent hypo perfusion of the brain, myocardium and both kidneys.
Etiology
In 90% of cases, hypertensive crises are a consequence of a longstanding, uncontrolled primary/essential hypertension
>low adherence
>high sodium diet
Other potential causes include:
- Stimulant intoxication
- Withdrawal symptoms
- Uncontrolled causes of secondary hypertension
- Intake of MAOIs with tyramine-rich food
- Acute SC injury or head trauma
- Stimulant intoxication - 1)cocaine 2) metamphetamine 3) phencyclidine
- Withdrawal symptoms - form abrupt cessation of antihypertensives such as CLONIDINE and B-blockers
- Uncontrolled causes of secondary hypertension
- renal parenchymal disease; AGN, CKD
- renovascular disease - renal artery stenosis
- pheochromocytoma
- cushing’s syndrome
- primary hyperaldosteronism
- coarctation of the aorta
- obstructive sleep apnea
- Intake of MAOIs with tyramine-rich food
- Acute SC injury or head trauma - autonomic dysreflexia
Pathogenesis
In normotensive individuals, there is ordinarily a broad range of pressures, about MAP at 60 to 180 mmHg through which arterioles and arteries can dilate or constrict to maintain normal and consistent perfusion pressures.
Thus, when blood pressure is acutely elevated, blood vessels reflexively CONSTRICTS to maintain normal perfusion pressures.
When the upper limit of author regulation is exceeded, blood vessels Cano longer constrict hands will overly dilate and rupture causing life-threatening hemorrhages.
On the other hand, when BP is acutely decreased, blood vessels will reflexively DILATE also to maintain normal organ perfusion pressures.
However, when the MAP goes below the limit of autoregulation, blood vessels will then collapse —> tissue ischemia.
In Chronic hypertensive individuals, the walls of the arteries in arterials have already undergone remodeling to accommodate chronic excessive pressure and shear stress. Autoregulation is disrupted and this limits the ability of the vessels to respond appropriately acute decreases increases in blood pressure.
When BP abruptly increases, larger arterials reflexively vasoconstrictor in an effort to limit pressure reaching at issues which would interfere with normal cellular activity
In this situation, acutely lowering the BP re-achieve a normal BP with reduce blood flow to tissues WITHOUT promt compensatory vasodilatation leading to and end-organ hypoperfusion
Again, It is important that blood pressure be lowered only operate by which tissue perfusion can be maintained by autoregulation
Clinical Manifestations
As mentioned hypertensive urgency is frequently a symptomatic and may only present with mild headache localized on the nape area which is easily relieved by intake of oral antihypertensive medication’s.
In contrast, hypertensive emergency will present with clinical manifestations of end organ damage which may include:
- Chest tightness or heaviness Radiating to the jar and left arm which may be due to myocardial infarction. PE: Weak s1, cold-clammy extremities
- Dyspnea, orthopnea or heaviness and easy fatiguability which may due to HEART FAILURE and PULMONARY EDEMA. PE: Distended neck veins, weak pulses, bibasal crackles
- Generalize neurologic symptoms such as agitation, delirium, stupor, seizures, visual disturbances as well as signs of increased intracranial pressure such as severe headache, nausea, vomiting and diplopia which may point to HYPERTENSIVE ENCEPHALOPATHY
- Focal neurologic science which could be due to an ischemic or hemorrhagic stroke
- Sharp lancinating pain on the chest or abdomen which radiates to the back end AAA
- New onset hematuria and proteinuria with creatinine elevation in HYPERTENSIVE NEUROPATHY
- Fresh soft and hard accidents, flame shaped hemorrhages and papilledema in HYPERTENSIVE RETINOPATHY
- ECLAMPSIA in pregnancy
Diagnosis
Diagnosis of hypertensive crisis is clinical based on accurate BP measurement of more than or equal to 180/120
Differentiation between hypertensive urgency an emergency is based on the presence or absence of signs and symptoms of end organ damage
Laboratory and ancillary exams requested to primarily determine the extent of and organ damage to guy treatment decisions
This is because certain Oregon dysfunctions may be a relative contraindication for starting certain antihypertensives
12-lead ECG Must be requested to investigate for myocardial infarction or ischemia. May also suggest electrolyte abnormalities and chamber enlargement.
INFARCTION:
> or = 2mm ST elevation (V2-V3) in MEN >40 yo
> or = 1.5mm ST elevation (V2-V3) in WOMEN
> or = 1 mm ST elevation (other contiguous chest leads)
ISCHEMIA:
> or = 1 mm ST depression in 2 or more contiguous leads
> or = 5 mm deep T wave inversions in 2 or more contiguous leads
Urinalysis should also be requested to screen for hematuria and proteinuria
Results should be correlated with serum creatinine and albumin – creatinine ratio should be computed as well as estimated GFR
COCKCROFT-GAULT FORMULA***
EGFR (ml/min) = [(140-age) x BW in kg] / serum creatine mg/dl x 72]] x 0.85 if female
Chest x-ray should also be requested to investigate for heart failure and pulmonary edema if physical exam results are unequivocal
In patients with neurologic signs and symptoms, cranial CT scan is warranted to evaluate presence of infarct, hemorrhage or edema
Hey Siri electrolytes should be measured not only to guide correction but also the guide the choice of antihypertensive agent
Contrast-enhanced CT/MRI of chest if aortic dissection is suspected but rapid blood pressure lowering to <110 mmhg should not be dealyed.
Other test which can be requested include:
CBC to exclude microangiopathic hemolytic anemia
Toxicology screen (stimulant intoxication)
Endocrine testing (pheochromocytoma, cushing’s syndrome, primary hyperaldosteronism)
Management
In the setting of hypertensive urgency, the long-term target is to reduce the BP to <130/80 within 24 to 48 hrs or longer in low risk patients
However, during the first 2-4 hours, MAP should not be lowered by more than 25-30% to preserve adequate organ perfusion.* (so wag naman masyadong mababa)
Since the most common cause of hypertensive urgency is non-adherence to prescribe antihypertensives, reinstitution of prior medication will solve the problem.
In patients receiving subtherapeutic doses, increasing the dose is permitted.
However, in patients who are considered HIGH RISK blood pressure should be lowered preferrably within hours.
This include patients with known aortic or intracranial aneurysms.
- *Two oral medications can be used over a short period of time as rescue.
1. CLONIDINE 0.2 mg single dose
2. CAPTOPRIL 6.25 mg or 12.5 mg single dose - *Nifedipine should not be used because it causes unpredictable reduction in BP
After which, patient is observed for a few hours to ascertain a reduction in BP by 20-30 mmhg and sent home with longer-acting agents such as Amlodipine 5 to 10 mg once daily.
Patient is advised to follow-up within a few days
In patients with HYPERTENSIVE EMERGENCY, they must be admitted to an ICU for continuous-monitoring of BP and target organ damage.
Optimal pharmacotherapy depends upon the specific organ at risk and must be parenterally administered.
Tx for Hypertensive Encephalopathy
In hypertensive encephalopathy, MAP should be reduced by 25% over 8 hours
Labetalol, NIcardipine and Esmolol are the preferred medications.
Tx Acute Ischemic Stroke
Generally for acute ischemic stroke, antihypertensive medications are withheld unless the SBP is above 220 mmhg or DBP is above 120 mmhg or unless the patient is eligible for reperfusion therapy with tPA but BP is >185/100
Preferred medications are LABETALOL and NICARDIPINE
Tx Acute Intracranial Hemorrhage
Target MAP in patients with intracranial hemorrhage depends on the presence or absence of signs of increased ICP
(+) increased ICP, maintain MAP <130 mmHg (SBP < 180 mmhg)
(-) increased ICP, maintain MAP <110 mmHg (SBP<160 mmhg)
Preferred medications are labetalol and nicardipine
Tx Acute Coronary Syndrome
For ACS, treatment is indicated if the BP >160/100 and the BP must be reduced at least 20-30% from baseline
Thrombolytics are contraindicated if BP 185/100 relative contraindication
B Blockers (Labetalol) and Nitroglycerin are the preferred drugs
Tx Acute Heart Failure
For acute heart failure, preferred medications are Vasodilators (dec. afterload) (IV Nitroglycerin, IV Enalapril) in addition to Loop Diuretics to be titrated to achieve SBP <130 mmhg
Tx Acute Aortic Dissection
For acute aortic dissection, SBP must be lowered to <100 within 20 minutes
Preferred tx include combination of
Narcotics (Morphiin sulfate),
B-blockers (Labetalol, Metoprolol, Esmolol)
Vasodilators (Nicardipine, Nitroprusside)
B-blockage should precede vasodilators to prevent reflex tachycardia
Tx PREECLAMPSIA, ECLAMPSIA
In women with preeclampsia or eclampsia, SBP must be lowered to <140 during the first hour
Preferred meds are Hydralazine, Labetalol and Nicardipine
Magnesium So4 should also be given to avoid seizures
Nitroprusside, ACEIs, ARBs and renin inhibitors should never be used due to their teratogenic effects
Tx Pheochromocytoma
In pheochromocytoma, Phentolamine IV Bolus is given to lower SBP <140 during the first hour. Additional bolus doses may be given every 10 minutes as needed to achieve target BP
Afterwhich, B-blockers can be given for tachycardia
B-blockers should not be adminitsered until adequate a-blockade has been established to prevent exacerbation of hypertensive crisis
